Similar to the results with p-Akt, ΔmiR-UL36/112/148D infection resulted in enhanced phosphorylation of several Akt substrates compared to WT HCMV infection, including FOXO3a (Fig 5A and 5C) and PRAS40 (Fig 5B and 5D). This evidence concerns the gene AKT1S1 and cytomegalovirus infection.